Kuznetsov 2000 Transplant Proc: Difference between revisions
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|injuries=Ischemia-Reperfusion; Preservation | |injuries=Ischemia-Reperfusion; Preservation | ||
|organism=Rat | |organism=Rat | ||
|tissues=Cardiac | |tissues=Cardiac muscle | ||
|preparations=Intact Organ, Isolated Mitochondria | |preparations=Intact Organ, Isolated Mitochondria | ||
|topics=Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential | |topics=Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential | ||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
}} | }} | ||
Revision as of 04:51, 5 April 2012
| Kuznetsov AV, Brandacher G, Steurer W, Margreiter R, Gnaiger E (2000) Isolated rat heart mitochondria and whole heart as models for mitochondrial cold ischemia-reperfusion injury. Transplant Proc 32: 45. |
» PMDI: 10700961
Kuznetsov AV, Brandacher G, Steurer W, Margreiter R, Gnaiger E (2000) Transplant Proc
Abstract: SHORT cold ischemia times (of less than 6 hours) tolerated by the heart remain one of the major problems in heart transplantation. Damaged mitochondria lead to heart injury by the diminished cellular energy status, oxidative stress, disturbance of ion balance, cytochrome c release, and induction of apoptosis.1-3 Improved understanding of preservation parameters affecting the efficiency of heart storage requires specific models of cold ischemia/reperfusion (CIR) injury.4
• O2k-Network Lab: AT_Innsbruck_Gnaiger E
Labels:
Stress:Ischemia-Reperfusion; Preservation Organism: Rat Tissue;cell: Cardiac muscle Preparation: Intact Organ, Isolated Mitochondria
Regulation: Respiration; OXPHOS; ETS Capacity, Coupling; Membrane Potential
HRR: Oxygraph-2k
